Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.3 (HSD)
 3,464 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Incomplete masculinization due to a deficiency of 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) was investigated in siblings aged 4 years (Case 1) and 12 years (Case 2). Diagnosis was based on increased ratios of androstenedione (A) to testosterone (T) in blood, and impaired reduction of A to T by 17 beta-HSD in vitro in the testes. Impairment was total in Case 2 but partial in Case 1. Case 2 also showed deficient conversion of dehydroepiandrosterone (DHA) to androstenediol and of oestrone to oestradiol by 17 beta-HSD which were normal in Case 1. Oxidation of T to A by 17 beta-HSD and conversion of 17 alpha-hydroxyprogesterone to A by 17,20 desmolase were normal in the testes of both siblings. 3 beta-HSD conversion of DHA to A was normal in Case 1, but markedly increased in Case 2. In contrast to testicular findings, 17 beta-HSD reduction of A to T in genital skin fibroblasts from Case 2 was normal and diagnosis would not have been possible from studies of measurements of this enzyme in skin. The severity of the testicular 17 beta-HSD deficiency in the peripubertal compared with the prepubertal sibling suggests either considerable intra-familial variation in the extent of the enzyme defect or that puberty may aggravate this disorder. The normal reductive action of 17 beta-HSD in skin, despite impaired action in testes, suggests involvement of more than one iso-enzyme.
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PMID:Incomplete masculinization due to a deficiency of 17 beta-hydroxysteroid dehydrogenase: comparison of prepubertal and peripubertal siblings. 282 Jun 22

The effect of treatment with prolactin or bromocryptine on testicular steroidogenesis and serum hormone levels were studied in immature and mature bonnet monkeys. Leydig cells alone showed the presence of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) in normal immature and mature monkeys. Administration of prolactin increased the activity of 3 beta-HSD and 17 beta-HSD in Leydig cells from mature monkeys, and also increased the serum levels of testosterone. Bromocryptine treatment induced exactly the opposite effect. These changes occurred in the absence of any change in serum gonadotrophin levels. In immature monkeys, prolactin and bromocryptine had no significant effect. These results suggest a direct stimulatory effect of prolactin on testicular steroidogenesis in mature monkeys.
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PMID:Prolactin and Leydig cell steroidogenic enzymes in the bonnet monkey (Macaca radiata). 283 48

The role of membrane phospholipids in testicular androgen biosynthesis was investigated by monitoring the effects of phospholipase treatments on the activities of the steroid transforming enzymes. Androgen biosynthesis in untreated rat testicular microsomes was examined by monitoring the temporal appearance of pregnenolone metabolites and was found to proceed through the 4-ene route. When phospholipase A2 was included, the 5-ene steroids 17-hydroxypregnenolone and dehydroepiandrosterone (DHEA) were formed in greater quantities, and the production of 4-ene steroids was reduced indicating that the conversion of 5-ene steroids to the 4-ene configuration was inhibited by phospholipase A2 treatment. Phospholipase C, in addition to inhibiting this step, also inhibited the conversion of C21 steroids to C19 steroids. When the enzymatic steps were measured individually, phospholipase A2 inhibited 3 beta-hydroxysteroid dehydrogenase-isomerase (3 beta-HSD-Isomerase) with an ED50 of 73 mU/ml but had no effect on the activities of 17-hydroxylase, C-17, 20 lyase, or 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD). However, though phospholipase C treatment inhibited 3 beta-HSD-Isomerase, it caused less inhibition (the ED50 value was 149 mU/ml). Furthermore, 17-hydroxylase and C-17, 20 lyase activities were also inhibited by phospholipase C treatment (ED50 values were 410 and 343 mU/ml, respectively), but no effect on 17 beta-HSD was observed. The differences in the apparent phospholipid requirements of the steroidogenic enzymes provides the possibility that the metabolic fate of pregnenolone may be regulated by changes in the phospholipid composition of the microenvironment.
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PMID:Phospholipases modulate the rat testicular androgen biosynthetic pathway in vitro. 284 83

cDNA clones for 17 beta-hydroxysteroid dehydrogenase (17-HSD; EC 1.1.1.62) were isolated from a placental lambda gt11 expression library using polyclonal antibodies against placental 17-HSD. The largest cDNA contained 1325 nucleotides, consisting of a short 5'-noncoding segment, a coding segment of 987 nucleotides terminated by a TAA codon, and a 329 nucleotide long 3'-noncoding segment. The open reading frame encoded a polypeptide of 327 amino acid residues with a predicted Mr of 34853. The amino acid sequence of 23 N-terminal amino acids determined from purified 17-HSD agreed with the sequence deduced from cDNA. The deduced amino acid sequence also contained two peptides previously characterized from the proposed catalytic area of placental 17-HSD.
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PMID:Complete amino acid sequence of human placental 17 beta-hydroxysteroid dehydrogenase deduced from cDNA. 284 51

Type II estrogen-binding sites (type II EBS) have been demonstrated in human peripheral blood mononuclear cells (PBMC) using a whole cell assay with [6,7-3H]estradiol [( 3H]E2) as tracer. During whole cell incubations for 60 min at 37 C for type II EBS quantification, we found that PBMC contain 17 beta-hydroxysteroid dehydrogenase (17 beta HSD) activity, which led to errors in estimating type II EBS concentrations by diminishing, by about 70%, the amount of available labeled E2. On the other hand, after 150 min at 4 C only 16% of the tracer was converted to estrone. Thus, we measured the maximal steady state binding in PBMC by incubating the cells with [3H]E2 at 4 C for 150 min. Equilibrium binding analysis of PBMC yielded sigmoid saturation curves with a saturation point at a ligand concentration of about 40 nmol/L. Scatchard analysis of binding data yielded a concave plot, which together with a Hill coefficient of 2.13, suggests that the type II EBS may have multiple binding sites which display positive cooperativity. The apparent equilibrium dissociation constant (Kd), determined from the [3H]E2 concentration required for half-saturation, was about 22 nmol/L. The type II EBS were estrogen specific, as demonstrated by competition experiments. Only those steroids with estrogenic activity inhibited binding of [3H]E2; nonestrogenic steroids did not. The type II EBS were found to be 3S macromolecules based on analysis of postlabeled fractions prepared by sucrose density gradient centrifugation. The number of type II EBS in PBMC from normal women was highest during the late follicular-early luteal phase of the menstrual cycle. We conclude that human PBMC specifically take up, retain, and metabolize E2.
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PMID:Type II estrogen-binding sites and 17 beta-hydroxysteroid dehydrogenase activity in human peripheral blood mononuclear cells. 284 27

Steroidogenic enzyme activities in the left ovary and the testes of 9- to 15-day-old chicken embryos were measured, and development of the activities was compared between sexes. Activity of delta 5-3 beta-hydroxysteroid dehydrogenase coupled with delta 5-delta 4 isomerase in the ovary and in the testis was comparable, and did not change throughout the period examined. Activity of 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) in the ovary was similar to or higher than that in the testis, depending on substrates employed. In both gonads, 17 beta-HSD activity did not change or tended to decrease from 9 to 15 days of development. On the other hand, activities of 17 alpha-hydroxylase, C-17--C-20 lyase in the ovary were three to eight times those in the testis, and aromatase activity in the ovary was definitely higher than that in the testis at all stages examined. The activities of 17 alpha-hydroxylase, C-17--C-20 lyase, and aromatase significantly increased from 9 to 11 days only in the ovary. From 13 to 15 days, the activities of 17 alpha-hydroxylase and C-17--C-20 lyase markedly increased only in the testis. These results suggest that, in the gonads of developing chicken embryos, there are sexual differences in the regulation of 17 alpha-hydroxylase, C-17--C-20 lyase, and aromatase activities.
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PMID:Developmental changes of steroidogenic enzyme activities in the embryonic gonads of the chicken: the sexual difference. 284 54

Cytosol and nuclear estrogen receptors were detected in 73% and 89% of untreated endometriosis specimens, respectively. The corresponding figures for cytosol and nuclear progestin receptors were 94% and 100%, respectively. Compared with the endometrium, the concentrations in endometriosis tissue were low. The anatomic site, the severity of the disease, and the phase of the menstrual cycle had no significant influence on receptor concentrations in endometriosis tissue. The activities of 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) did not increase during the luteal phase. Danazol for 1, 3, 7 to 11, and 18 to 30 days, or medroxyprogesterone acetate for 5 days, had no effect on receptor concentrations or 17 beta-HSD activity in endometriosis tissue. The frequent presence of the receptors suggests that endometriosis lesions are under the control of steroid hormones. The lack of effect by progesterone and progestins on 17 beta-HSD shows that this regulation is different in endometriosis tissue and in the endometrium.
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PMID:Steroidal regulation of endometriosis tissue: lack of induction of 17 beta-hydroxysteroid dehydrogenase activity by progesterone, medroxyprogesterone acetate, or danazol. 298 48

The sensitivity of soluble, 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) of human placenta to inactivation by fatty acids was examined. Exposure to the unsaturated fatty acids oleic, arachidonic, linoleic and linolenic acid resulted in the loss of activity. Methyl and ethyl esters of oleic acid, the saturated fatty acid, stearic acid and prostaglandins E2 and F2 alpha were without effect. Inactivation by oleic acid required the fatty acid at levels above its critical micelle concentration, 50 microM, as estimated by light-scattering. Steroid substrates and inhibitors did not protect against inactivation. NAD+, NADH, NADP+ and NADPH did protect. The concentrations of NADP+, 50 microM, and NAD, 1.5 mM, necessary for complete protection were significantly greater than their respective Michaelis constants, 0.16 microM and 15.2 microM. The data suggest that soluble 17 beta-HSD can bind to fatty acid micelles and that the binding site(s) on the enzyme are at or near pyridine nucleotide binding sites.
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PMID:Inactivation of soluble 17 beta-hydroxysteroid dehydrogenase of human placenta by fatty acids. 299 30

Intratumoral activity of the enzyme 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) was measured in 55 patients with breast cancer (17 pre- and 38 post-menopausal) before and/or after 8 days of a progestin treatment (lynestrenol 10 mg/day). In 12 patients the 17 beta-HSD ability to be stimulated was compared to estradiol and progesterone receptor (ER and PR) levels. In premenopausal patients 17 beta-HSD was higher when tumorectomy was performed in the luteal phase than in the follicular phase. In post-menopausal patients, 17 beta-HSD is higher after progestin treatment. However 17 beta-HSD stimulation by lynestrenol depends on receptor levels. It is most after markedly stimulated in ER+ PR+ tumors. It remains low in ER- PR- tumors. In conclusion, intratumoral measurement of the progesterone dependent enzyme (17 beta-HSD) in breast cancer after progestin treatment provides a fine and reliable index of the presence and functional character of PR and hormone dependence of the tumor.
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PMID:[Evaluation of 17-beta-hydroxysteroid dehydrogenase activity as a marker of the hormone dependence of breast cancers]. 299 4

The effects of gestrinone (R 2323) on endometrial and endometriosis tissue concentrations of cytosol estrogen and progestin receptors and the activity of 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) were investigated in 11 patients operated on because of suspected external endometriosis. Serum concentrations of luteinizing hormone, follicle-stimulating hormone, estradiol (E2), progesterone, testosterone (T), and sex-hormone-binding globulin (SHBG) were also investigated. After one control cycle, the patients received 2.5 mg of oral gestrinone twice weekly from the fifth day of the first treatment cycle until the eighth day of the second treatment cycle, the day of operation being day 10. Treatment with gestrinone decreased serum concentrations of T during the second treatment cycle and effected a major decrease in SHBG during both treatment cycles, resulting in highly increased free T and free E2 indices. The effects of gestrinone on the endometrium, a decrease in estrogen and progestin receptors, and induction of 17 beta-HSD are characteristic progestin actions. These parameters remained unchanged in endometriosis tissue. Our data indicate that gestrinone has effects that are typical of androgens and progestins in patients with endometriosis.
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PMID:Effect of gestrinone in endometriosis tissue and endometrium. 299 49


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